Maternal diet, prenatal exposure to dioxins and other persistent organic pollutants and anogenital distance in children

Abstract

We investigated the potential endocrine disruptive effect of prenatal exposure to persistent organic pollutants (POPs) through maternal diet, by measuring anogenital distance in newborns and young children. We included 231 mothers and their newborns measured at birth from the Rhea study in Crete, Greece and the Hmar study in Barcelona, Spain and 476 mothers and their children measured between 1 and 2 years from the Rhea study. We used food frequency questionnaires to assess maternal diet and estimated plasma dioxin-like activity by the Dioxin-Responsive Chemically Activated LUciferase eXpression (DR-CALUX®) and other POPs in maternal samples. We defined a "high-fat diet" score, as a prenatal exposure estimate, that incorporated intakes of red meat, processed meat, fatty fish, seafood, eggs and high-fat dairy products during pregnancy. Increasing maternal "high-fat diet" score was related to increasing dioxin-like activity and serum concentrations of lipophilic persistent organic pollutants in maternal blood. An inverse dose-response association was found between "high-fat diet" score and anoscrotal distance in newborn males. The highest tertile of the maternal score was associated with -4.2 mm (95% CI -6.6 to -1.8) reduction in anoscrotal distance of newborn males, compared to the lowest tertile. A weak positive association was found between the "high-fat diet" score and anofourchetal distance in newborn females. In young children we found no association between maternal "high-fat diet" score and anogenital distances. In conclusion, maternal high-fat diet may be linked to high prenatal exposure to persistent organic pollutants and endocrine disruptive effects, resulting to phenotypic alterations of the reproductive system.

Anogenital distance and reproductive parameters in young men

“…The rapid pace of the increase in such reproductive disorders suggests that environmental or life style factors, rather than an accumulation of genomic structural defects, are the most likely causes (Skakkebaek et al ., ). AGD AP measurements have been associated with prenatal exposure to endocrine disruptors (Swan et al ., ; Miao et al ., ; Bustamante‐Montes et al ., ; Papadopoulou et al ., ; Vafeiadi et al ., ) or prostate cancer (Castaño‐Vinyals et al ., ). AGD AS measurements have been associated with semen quality and serum reproductive hormones (Eisenberg et al ., , ; Mendiola et al ., ).…”

“…It may be used as a retrospective measure of foetal androgen exposure during the masculinisation programming window (Hsieh et al ., ; Scott et al ., ). In humans, prenatal exposures to endocrine disruptors, such as phthalates (Swan et al ., ; Suzuki et al ., ; Bustamante‐Montes et al ., ), dioxins, DDT metabolites or bisphenol‐A (Torres‐Sanchez et al ., ; Miao et al ., ; Papadopoulou et al ., ; Vafeiadi et al ., ) have been linked to shorter AGD in children. Additionally, boys with hypospadias and cryptorchidism have shorter AGD (Hsieh et al ., , ; Jain & Singal, ; Thankamony et al ., ).…”

Effect-based assessment of persistent organic pollutant and pesticide dumpsite using mammalian CALUX reporter cell lines

“…The (semi-)quantitative nature of the data 3. A reduced risk of underestimation of the actual hazard by directly measuring sum activities instead of focusing the presence of individual compounds that are among the Busual suspects similar approach as the one presented here for soil quality assessment may also be used for other environmental compartments, and other types of samples such as sediments, food and feed, and animal and human tissue (e.g., Suzuki et al 2011;Papadopoulou et al 2013;Porpora et al 2009). …”

Dichlorodiphenyltrichloroethane exposure and anogenital distance in the Venda Health Examination of Mothers, Babies and their Environment (VHEMBE) birth cohort study, South Africa

“…Anogenital distance has been examined in humans in relation to fetal exposures to various endocrine-disrupting chemicals such as phthalates (Swan et al, 2005, 2015; Suzuki et al, 2012; Bustamante-Montes et al, 2013; Bornehag et al, 2015); dioxin (Papadopoulou et al, 2013b; Vafeiadi et al, 2013), and bisphenol A (Miao et al, 2011), and the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT) and its metabolite, dichlorodiphenyldichloroethylene (DDE) (Longnecker et al, 2007; Torres-Sanchez et al, 2008). In boys, elevated prenatal phthalate exposure was associated with shorter AGD, suggesting an antiandrogenic effect (Swan et al, 2005, 2015; Suzuki et al, 2012; Bustamante-Montes et al, 2013; Bornehag et al, 2015).…”